Department of Sports Medicine Center, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Department of Blood Transfusion, Xinqiao Hospital, Army Medical University, 400037, Chongqing, China.
BMC Musculoskelet Disord. 2021 Nov 15;22(1):949. doi: 10.1186/s12891-021-04838-w.
Tendon diseases and injuries are a serious problem for the aged population, often leading to pain, disability and a significant decline in quality of life. The purpose of this study was to determine the influence of aging on biochemistry and histology during tendon healing and to provide a new strategy for improving tendon healing.
A total of 24 Sprague-Dawley rats were equally divided into a young and an aged group. A rat patellar tendon defect model was used in this study. Tendon samples were collected at weeks 2 and 4, and hematoxylin-eosin, alcian blue and immunofluorescence staining were performed for histological analysis. Meanwhile, reverse transcription-polymerase chain reaction (RT-PCR) and western blot were performed to evaluate the biochemical changes.
The histological scores in aged rats were significantly lower than those in young rats. At the protein level, collagen synthesis-related markers Col-3, Matrix metalloproteinase-1 and Metallopeptidase Inhibitor 1(TIMP-1) were decreased at week 4 in aged rats compared with those of young rats. Though there was a decrease in the expression of the chondrogenic marker aggrecan at the protein level in aged tendon, the Micro-CT results from weeks 4 samples showed no significant difference(p>0.05) on the ectopic ossification between groups. Moreover, we found more adipocytes accumulated in the aged tendon defect with the Oil Red O staining and at the gene and protein levels the markers related to adipogenic differentiation.
Our findings indicate that tendon healing is impaired in aged rats and is characterized by a significantly lower histological score, decreased collagen synthesis and more adipocyte accumulation in patellar tendon after repair.
肌腱疾病和损伤是老年人群体的一个严重问题,常导致疼痛、残疾和生活质量的显著下降。本研究旨在确定衰老对肌腱愈合过程中生物化学和组织学的影响,并为改善肌腱愈合提供新策略。
本研究共纳入 24 只 Sprague-Dawley 大鼠,平均分为青年组和老年组。建立大鼠髌腱缺损模型,分别于术后 2 周和 4 周取材,行苏木精-伊红(H&E)、阿利新蓝(Alcian blue)和免疫荧光染色进行组织学分析。同时采用反转录-聚合酶链反应(RT-PCR)和 Western blot 检测生物化学变化。
老年大鼠的组织学评分明显低于青年大鼠。在蛋白水平,与胶原合成相关的标志物 Col-3、基质金属蛋白酶-1(MMP-1)和金属蛋白酶抑制剂-1(TIMP-1)在老年大鼠第 4 周时的表达均低于青年大鼠。虽然老年肌腱的软骨形成标志物聚集蛋白聚糖(aggrecan)在蛋白水平的表达降低,但第 4 周的 Micro-CT 结果显示两组间异位骨化无显著差异(p>0.05)。此外,我们发现老年肌腱缺损处有更多的脂肪细胞积聚,油红 O 染色和基因及蛋白水平的脂肪细胞分化相关标志物也证实了这一点。
本研究结果表明,老年大鼠的肌腱愈合受损,其特征为组织学评分显著降低、胶原合成减少以及髌腱修复后脂肪细胞积聚增加。